Accelerated cell death genes

Mach JM, Castillo AR, Hoogstraten R, Greenberg JT (2001) The Arabidopsis Accelerated Cell Death Gene ACD2 Encodes Red Chlorophyll Catabolite Reductase and Suppresses the Spread of Disease Symptoms. Proc Natl Acad Sci USA 98 771... 

Pruzinska A, Tanner G, Anders I, Roca M, Hortensteiner S (2003) Chlorophyll Breakdown Pheophorbide a Oxygenase is a Rieske-type Iron-sulfur Protein, Encoded by the Accelerated Cell Death 1 Gene. Proc Natl Acad Sci USA 100 15259... 

Ads with mutations in the E1B/19K gene exhibit the cytideg phenotype, which is characterized by accelerated cell death, large plaques, and degradation of viral and cellular DNA. This suggested that E1B/19K is involved in apoptosis prevention (Chinnadurai 1998). Accumulating evidence suggests that E1B/19K interferes with both p53-dependent and p53-independent apoptosis pathways. Multiple mechanisms have been proposed by which E1B/19K counteracts apoptosis however, the exact mechanism remains unknown. 

GPI-deficient mammalian cells are viable in tissue culture and many GPI-deficient mutant cell lines have been established. However, GPI deficiency has major consequences at the level of tissues and the whole body. This was revealed in transgenic mouse models in which the PIG-A gene (required for the first step of GPI biosynthesis) was knocked out in specific tissues or in the whole animal. For example, keratinocyte-specific disruption of PIG-A caused abnormal development of skin leading to death of the mutant mice a few days after birth (M. Tarutani, 1997), and disruption of PIG-A in the whole animal resulted in embryos that did not develop beyond day 9 of gestation (M. Nozaki, 1999). A somatic mutation of PIG-A in multipotent hematopoietic human stem cells causes paroxysmal nocturnal hemoglobinuria, an acquired hemolytic disease in humans characterized by abnormal activation of complement on erythrocytes due to a deficiency of GPI-anchored complement regulatory proteins such as decay accelerating factor (N. Inoue, 2003). This disease is characterized by intravascular hemolysis and anemia. 

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